The object of the proposed study will be to devise techniques to detect and define qualitative alterations in the steroid secretion of aldosterone-producing tissue. We will consider inborn errors of biosynthesis leading to clinical aldosterone deficiency as well as circumstances in which the biological activity of accumulated intermediates determines the clinical picture. In the latter category may be certain hypertensive syndromes in which the secretion of a mineralocorticoid other than aldosterone or 11-deoxycorticosterone is suspected.